Eaton agent, the microbe
that has been associated with atypical pneumonia, was originally thought to be
a virus because certain antibiotics were not effective and it was so much
smaller than cell wall form bacteria.†
It was found to have one of the smallest genomes among bacteria and
belongs to the Class: Mollicutes, Order: Mycoplasmatales, Genus: Mycoplasma,
Species: Pneumoniae.† Mycoplasma
Pneumonia.† A related Mycoplasma
is M. hominus that Drs Brown and Clark associated with rheumatic
arthritis. Clarkís pictures are of M. hominis, not M. pneumonia† (MP).

SUMMARY

The detailed structure is depicted
in M.
pneumonia genetic summary†
reported by NewScientist with a detailed
electron-tomograph picture showing remarkable detail in color. That picture
of M. pneumonia bacteria shows smaller body components, like ribosomes, chromosomes, or mitochondrial organelles
that bound and enable molecular chemical transformations in host cells, driven
by the DNAsí, RNAsí and now XNAsí
recipe-templatesí codons. †MP
invades epithelial cells in the respiratory tract and contributes to COPD
respiratory inflammation and bronchitis. MPinvades
erythrocytes (RBCs) and also invades immune cells,
(phagocytes) leading to suppression of immune functions.† Invaded host epithelial and blood cells act
as replication factories for the obligate microbes, similar to the way viruses
replicate.

MP Pathology in Detail

Pathology is complex for M.
pneumonia, other Mycoplasmas (M. hominis, fermentans, et al),† and other persistent, obligate
microbes.† The first order symptomology
of MP is pneumonia, bronchitis and COPD.† Since MP is persistent, COPD is episodic. Since the human
herd is near 100% infected by Chlamydia pneumoniae,† and RSV (respiratory syncytial virus) the
other persistent microbes can† all work
together to infiltrate immune cells, to suppress immune system functions and to
infect/invade† blood and epithelial
cells in various other parts of the body.

∑Mycoplasmas can also disrupt the hostís immune
system. They can stimulate lymphocytes to secrete inflammatory cytokines, which
lead to inflammation and both stimulation and/or suppression of the immune
system.

∑Mycoplasmas leaving an infected cell incorporate
hostís cell surface material into their own surface structure, they can
instigate an autoimmune response. Meanwhile the emerging mycoplasmas can evade
the immune system by hiding inside host cells or fusing with the host cellular
membranes.

Mycoplasmas can also invade
the epithelial lining of blood vessels, where they appear to facilitate the
release of molecules that can cause vasculitis (inflammation) and the formation
of plaque inside blood vessel wall surfaces. In the absence/shortage of
protecting vitamin C and Lysine† See Pauling Case
History.

Mycoplasmas Shape Change to multiple forms:

Mycoplasmas and other persistent microbes are
equipped to change shapes and form, appearing then disappearing, changing
shape, shuffling their surface elements, invade host cells, then hang out as
normal flora coated with molecules taken from the cells they invaded. They even
have protective forms to defeat antibiotics and some can shift to this form in
a few short minutes as seen in vitro under a microscope.† Pulsing the antibiotic can multiply-attrite
the shape-changing microbes, but this pulsing protocol is not widely followed.
It should be.

MP are pleomorphic
(structurally changing). In place of rigid cell walls, they have flexible lipid
(water insoluble fat) outer surfaces. Like amoebas they bend and move,
squeezing into tight spaces. They are so small they slide through laboratory
and hospital filters used to produce or maintain bacterial sterility -- making
them one of the most common contaminants in diagnostic laboratories and vaccine
manufacturing.

Mycoplasmas Contaminate other Vaccines:

They grow in the same live cell media used to grow
virus vaccines.† In one recent study of
vaccines, mycoplasmas were found to contaminate about six percent of commercial
vaccines.† As contaminants of both live
and killed vaccines, their presence can generate an unintended immune response.

Past trials of experimental M.
pneumonia vaccines were reported as dangerous failures. The tested MP
vaccines both did not protect, but they also generated a significant fraction
of life-threatening, very strong immune/inflammation reactions to the wild
mycoplasma test challenge forms. So mycoplasma †vaccine contamination makes the vaccines
dangerous for a significant† (~5%)
fraction of those inoculated. Total risk factor is .05*.06= .003 or .3% or 3 in
1000 cases.† Live MMP vaccines
contaminated with mycoplasmas, †can infect the vaccinated. Cases of infected live virus vaccines
documented in the literature include contamination with HIV, SIV, parvovirus,
measles, smallpox and polio strains that lead to

Mycoplasmas infect
everything including animals, plants, and possibly other microbes. Generally,
strains have adapted to specific host species, with some exceptions. Garth
Nicolson the pets of GWI or CFS patients exhibited similar symptoms as their
owners, and then tested positive for the same mycoplasmas. They are highly
contagious, but not all infected show noticeable symptoms. Transmission occur
among people in close proximity (families, classmates, etc).

HOW MYCOPLASMAS INTERACT IN THE BODY

Mycoplasmas invade the
cells of the host (patient) and oror to attach-to or imbed-into the outside of
host cells.

They depend on host cells for
nutrients such as cholesterol, certain amino acids, etc. They compete with the
host cells for these nutrients and energy which can interfere with host cell
functions. Fatigue is one symptom.

†A mycoplasma has very little DNA of its own, but is capable
of using/controlling DNA from an invaded cell causing that cell to malfunction
in many significant ways (mitochondrial dysfunction) and/or die, or invasion
can cause inflammation and DNA/RNA mutation and damage of the host cells.

†Mycoplasmas attach to host cells with a tiny arm coated in
protein which attaches to the protein coating of host cells. For this reason,
antibiotics like tetracycline, which are classified as "protein synthesis
inhibitors" are often used against mycoplasma infections. While these
antibiotics may block this protein attachment and very slowly starve it from
the nutrients it needs from host cells to thrive and replicate, it still takes
a healthy immune system to actually kill the mycoplasma for good. Better
nutrition, especially vitamin C in high consistent levels, can stimulate
invaded cell apoptosis (death).

†Mycoplasmas are highly adaptable to changing environments
and can move anywhere in the body, attaching to or invading virtually any type
of cell in the body that has a shape that matches the form of its protein
hooks.

†The mycoplasma adhesion proteins are very similar to human
proteins. Once adhered to the host cell, the mycoplasma can completely mimic or
copy the protein cell of the host cell. This can cause the immune system to
begin attacking the body's own cells, diagnosed as an autoimmune disease.

†Certain Mycoplasma species can either activate or suppress
host immune systems, and they may use these activities to evade host immune
responses. Mycoplasmas can turn on the chain reaction immune responses.
This includes the generation of pro-inflammatory cytokine molecules which are
found in inflammatory disorders, called autoimmune diseases.

†Mycoplasma can signal and attract immune system phagocytes
(natural killer NK cells) that are supposed to eat them. Inside these
phagocytes, they can make copies of themselves and† be carried to new locations of inflammation.

†When a mycoplasma attaches to a host cell, it generates and
releases hydrogen peroxide and superoxide Nitrogen and Reactive Oxygen Species,
AKA free-radicals, (NOS and ROS) and these (hy)peroxides damage cells organs,
tissues, mitochondria, and DNA/RNA, aging the host.† Vitamin C is the antidote.